tag:blogger.com,1999:blog-549949223388475481.post4962996217487107538..comments2024-03-19T02:33:29.499-05:00Comments on Dr. Smith's ECG Blog: Syncope, Hypotension, and a Large Right Ventricle -- What is the ECG Diagnosis?Unknownnoreply@blogger.comBlogger11125tag:blogger.com,1999:blog-549949223388475481.post-19779848277653896702016-09-07T16:28:02.578-05:002016-09-07T16:28:02.578-05:00Yes, but difficult with bedside ultrasoundYes, but difficult with bedside ultrasoundSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-89550696964907503612016-09-07T00:14:19.186-05:002016-09-07T00:14:19.186-05:00RV wall thickness by echo may be helpful in dd of ...RV wall thickness by echo may be helpful in dd of acute or chronic pulmonary hypertension.Anonymousnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-41253977514798478292016-09-04T10:52:35.758-05:002016-09-04T10:52:35.758-05:00Not totally certain, but I suspect there was a per...Not totally certain, but I suspect there was a period of hypotension from temporary RV failure. This leads to extremely poor RV perfusion (RV is perfused during systole; if there is hypotension at the same time it is pumping against 70 mmHg, there is no perfusion of RV myocardium). Low RV perfusion at the same time that the RV has to pump against very high pulmonary artery pressure leads to some RV myocardial cell loss.<br />Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-27938060868354300062016-09-03T11:55:33.577-05:002016-09-03T11:55:33.577-05:00Why increased TnI level?Why increased TnI level?Glebnoreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-72145250188504966222016-09-03T09:12:51.782-05:002016-09-03T09:12:51.782-05:00Great comments, Ken. thanks. The computer measur...Great comments, Ken. thanks. The computer measurement of the QRS was 110 ms (this is one thing computers are accurate at), so incomplete RBBB at best. The QT and QU are indeed long, and much longer than the previous ECG (not shown), and these certainly can be due to low Mg, but K of 3.4 is not very low. RVH is definitely hard to diagnose on ECG in the presence of incomplete RBBB.<br />SteveSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-4687671268153210522016-09-02T15:03:13.624-05:002016-09-02T15:03:13.624-05:00Excellent case! — albeit one that my opinion about...Excellent case! — albeit one that my opinion about this ECG differs slightly. KEY points brought out by this case (and its accompanying ECG) are the following: i) The HPI ( = History of Present Illness) is an indispensable part of clinical management. This older adult with syncope and initial unresponsiveness had recent poor oral intake and vomiting (ie, a set-up for volume depletion); ii) The PMH ( = Past Medical History) is equally essential to assessment — this patient was found to have chronic cor pulmonale and prior Echo showing marked RVH, pulmonary hypertension but a normal LV; and iii) Use of stat Echo may prove invaluable — great picture here of a markedly dilated hypocontractile RV with associated good LV contractility.<br /><br />I interpreted this tracing as showing RBBB (or at the least, incomplete RBBB). I measure the QRS as between 0.11-0.12 second (in V1,V2) — with wide terminal S waves in leads I and aVL. Clearly, there are some atypical features here for RBBB — namely lack of an initial upright deflection (r wave) in lead V1, and lack of a wide terminal S wave in lead V6 — but not all RBBBs fit textbook description. Right-terminal delay is suggested by the wide terminal S in limb leads and the tall R in V1. That said, diagnosis of combined RVH and RBBB is challenging under the best of circumstances. Some electrocardiographers suggests excessive height of the R’ deflection in lead V1 (beyond 8, 10 or 15mm) makes that diagnosis — but my reservation has always been that with pure RBBB, the RV depolarizes unopposed, rendering numerical criteria far less objective for detecting true RV chamber enlargement from ECG. Presence of clear RAA in association with a tall R in V1 correlates well with anatomic RVH (since only one condition, which is rare [ = tricuspid stenosis] produces RAE but not RVH) — but the P wave in this tracing lacks the height and pointedness that typically characterizes RAE.<br /><br />Of note, the QTc in this tracing is LONG — and in my opinion, far longer than should be expected simply from RVH and/or RBBB. In addition, there is ST depression in V2-thru-V5, with what is probably a large U wave in leads V2-thru-V5. This correlates clinically with hypokalemia and the marked hypomagnesemia that this volume-depleted patient had — and further complicates assessment of this ECG.<br /><br />BOTTOM LINE: Putting all ‘pieces” of the clinical presentation here together — Dr. Smith makes a strong case for primary volume depletion as the precipitating event — which was supported by dramatic clinical improvement with volume repletion. I think it would be hard to be certain as to whether the tracing shown here represents pure RVH (from chronic cor pulmonale with pulmonary hypertension) vs combined conduction defect + RVH — unless one was able to do sequential review of this patients series of prior ECGs over the years to see which ECG features developed when … So while I’ll suggest that we do have evidence of an RV conduction defect here (at the least, incomplete rbbb) — that point is academic, and pales in importance to recognition of how PMH, HPI, Echo in the ED + ECG interpreted in context to the complete clinical situation are the essentials for optimal clinical management. THANKS to Dr. Smith for presenting this excellent case!ECG Interpretationhttps://www.blogger.com/profile/02309020028961384995noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-30829759782821707052016-09-02T11:39:36.436-05:002016-09-02T11:39:36.436-05:00K = 3.4. Mg = 1.3. Might be related.K = 3.4. Mg = 1.3. Might be related.Steve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-17849693279171721022016-09-02T11:37:15.066-05:002016-09-02T11:37:15.066-05:00You still need to consider PE, but with skepticism...You still need to consider PE, but with skepticism. Use d dimer. Do careful history. In this case, the history brought up the likelihood of dehydration. Orthostatics could have confirmed it. Fluid replacement would have resolved the issue. If you're still worried, you may still need CTPA, but your index of suspicion should be much much lowerSteve Smithhttps://www.blogger.com/profile/08027289511840815536noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-48822491924406774632016-09-02T07:37:24.131-05:002016-09-02T07:37:24.131-05:00Downup T wave with long QT in chest leads
What...Downup T wave with long QT in chest leads <br />What's the S.K, S.Mg Sheikh iliyashttps://www.blogger.com/profile/07205705977848528507noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-50228394927932872452016-09-01T18:28:45.050-05:002016-09-01T18:28:45.050-05:00history and serial ecg's(old ecg's in this...history and serial ecg's(old ecg's in this case) provide context, this illustrates the limitation of of dx on one ecgAnonymoushttps://www.blogger.com/profile/05540000170929817989noreply@blogger.comtag:blogger.com,1999:blog-549949223388475481.post-9159802047497746392016-09-01T10:53:03.041-05:002016-09-01T10:53:03.041-05:00thanx sir
hw can we differentiate b/w p.e n RVH in...thanx sir<br />hw can we differentiate b/w p.e n RVH in this setting as u pointed out sinus tachycardia,RAD,S1Q3T3,hypotension.wht specific features n history should b sought out for p.e??Anonymoushttps://www.blogger.com/profile/13759286213686182998noreply@blogger.com